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Stack #4584173
NEURAL TUBE DEFECTS
| Term | Definition 1 | Definition 2 |
|---|---|---|
| Major Events in Human Brain Development and Peak Times of Occurrence - 1 to 2 wks | • Pre-embryonic • Zygote to • Implantation to • Bilaminar to • Embryo | |
| Major Events in Human Brain Development and Peak Times of Occurrence - 3 to 4 wks | • Neurulation • Neutral tube to • Brain and Spinal cord, Neural crest to • PNS and leptomeninges | |
| Major Events in Human Brain Development and Peak Times of Occurrence - 2 to 3 mos | • Prosencephalic • Paired cerebral hemispheres, LV, BG, Thalami, Optic Nerves/chiasm CC, SP | |
| Major Events in Human Brain Development and Peak Times of Occurrence - 3 to 4 mos | • Neuronal Proliferation • Full complement of neurons in cerebral hemispheres | |
| Major Events in Human Brain Development and Peak Times of Occurrence - 3 to 5 mos | • Neuronal Migration • Formation from 3 layered embryonic cortex to 6 layered adult cortex | |
| Major Events in Human Brain Development and Peak Times of Occurrence - 5 mos to postnatal yrs | • Organization • Axonal and dendritic elaboration • Synaptogenesis • Programmed Cell death | |
| Major Events in Human Brain Development and Peak Times of Occurrence - Birth to Postnatal yrs | • Myelination • Formation of myelin | |
| Anterior neuropore | closes on day 25 | |
| Posterior neuropore | closes on day 28 | |
| NORMAL DEVELOPMENT • The process of neurulation | is completed by the end of the first month of embryonic development. | |
| NORMAL DEVELOPMENT • Expansion of the cranial brain structures via development of a primitive ventricular system is accomplished by... | temporary occlusion of the caudal (spinal) neural tube (days 23–27), which creates a rostral enclosed fluid-filled space, thus providing pressure to expand the cranial lumen, providing the impetus for brain enlargement. | |
| NORMAL DEVELOPMENT • Neural crest cells, precursors to cell types such as melanocytes, Schwann cells, dura matter, and dorsal root, as well as autonomic ganglion, | are thought to arise during this same time from the neural tube near the junction between neuroectoderm and cutaneous ectoderm. | |
| NORMAL DEVELOPMENT • Neural induction | involves numerous soluble, diffusible factors produced by a variety of genes (eg, sonic hedgehog), specific cells surface signaling molecules important for appropriate migration of cells within the developing neural tube, and direct cell–cell signaling | |
| ASCENDING PATHWAYS | LATERAL SPINOTHALAMIC TRACT ANTERIOR SPINOTHALAMIC TRACT POSTERIOR WHITE COLUMN POSTERIOR SPINOCEREBELLAR TRACT ANTERIOR SPINOCEREBELLAR TRACT CUNEOCEREBELLAR TRACT | SPINOTECTAL TRACT SPINORETICULAR TRACT SPINO-OLIVARY TRACT VISCERAL SENSORY TRACTS |
| DESCENDING PATHWAYS | CORTICOSPINAL TRACTS RETICULOSPINAL TRACTS TECTOSPINAL TRACT RUBROSPINAL TRACT VESTIBULOSPINAL TRACT OLIVOSPINAL TRACT ? DESCENDING AUTONOMIC FIBERS | |
| DYSRAPHIC DEFECTS - Anterior neuropore | • Anencephaly • Encephalocoele • Chiari I malformation | |
| DYSRAPHIC DEFECTS - Posterior neuropore | • Spina bifida occulta • Spina bifida cystica | |
| SPINA BIFIDA | • 2nd most common disability in children • Folic acid fortification can alter a woman’s risk of an NTD-affected birth from 50% to 70%. | |
| SPINA BIFIDA AAP | • All women of childbearing age: 400 micrograms/day • Women w/ a previous NTD pregnancy: 4000 micrograms/day one month prior to conception and through the first trimester • If one parent has spina bifida, the risk is 4% with a similar disorder. | • High-risk pregnancies (mothers taking valproic acid or has diabetes): 4 milligrams/day • Most children are born to families w/o a prior affected child (0.1%–0.2%) • Risk for recurrence: one child w/ NTD is 2%-5% and up to 10%-15% if two siblings |
| SPINA BIFIDA ETIOLOGY | • Multifactorial • Neural tube closure failure during embryonic development | |
| SPINA BIFIDA PATHOLOGY | • Primary failure of neurulation → prevents the mesoderm adjacent to the notochord from forming muscle and bone (ie, via somitic mesoderm), which normally forms around the tube to protect it. | • Failures of induction of NT by the notochord can result in incomplete CNS development and/or overgrowth of CNS precursors |
| SPINA BIFIDA Other proposed mechanisms: | Failure of Henson’s node to lay down the notochord correctly that causes significant errors in induction of the neural tube | |
| Defective closure of rostal neuropore | 1. incomplete development of brain with degeneration 2. Incomplete development of calvaria 3. Alteration in facies (facial apperance) +/- auricle | |
| Neural deficit caudal to lesion | +/- Clubfoot | |
| Meningomyelocele | +/- Hydrocephalus | |
| Unfused vertebral arch | Spina bifida occulta | |
| Meroencephaly | partial absence of brain, results from defective closure of rostal neuropore | |
| Meningomyelocele | results from defective closure of caudal nueropore | |
| SPINA BIFIDA GENETIC INFLUENCES | • Higher rate among females • Consanguinity among parents of individuals with NTD • Previous affected pregnancy – three to fivefold higher risk of recurrence | • Mutations/polymorphisms in the enzyme 5,10-methylenetetrahydrofolate reductase (MTHFR) • Elevated homocysteine levels in pregnant women |
| SPINA BIFIDA ENVIRONMENTAL INFLUENCES 1 | • Hyperthermia during early pregnancy—the first 28 days during which neurulation occurs • Exposure to solvents • Lowered intake of foods containing folate in the diet • Disorders of absorption of folate in the intestine | • Women with the genetic disorder of zinc metabolism acrodermatitis enteropathica • Maternal obesity and associated diabetes • Cigarette smoking • Valproic acid taken for seizures during pregnancy |
| SPINA BIFIDA ENVIRONMENTAL INFLUENCES 2 | • Use of highly active antiretroviral therapy (HAART) in the treatment of human immunodeficiency (HIV) disease • Drugs associated with NTDs: isotretinoin (Accutane); etretinate (Tegison); and anticancer agents such as methotrexate. | • Fetal alcohol syndrome • Some chromosomal disorders: Trisomy 21 (Down’s syndrome) and trisomy 13 (Patau syndrome) |
| isotretinoin (Accutane) | used for acne treatment | |
| etretinate (Tegison) | psoriasis treatment | |
| SPINA BIFIDA RISK FACTORS - History NTD in another child | RR - 30 | |
| SPINA BIFIDA RISK FACTORS - Low folate | RR 2-8 | |
| SPINA BIFIDA RISK FACTORS - Diabetes (pregestational) | RR 2-10 | |
| SPINA BIFIDA RISK FACTORS - VPA and carbamazepine | RR 10-20 | |
| SPINA BIFIDA RISK FACTORS - Maternal Obesity | RR 1.5-3.5 | |
| SPINA BIFIDA PRENATAL SCREENING | • Quad screen (alpha feto-protein (AFP), human chorionic gonadotropin (HCG), estriol, and inhibin A) is done in the second trimester. • Elevated levels of AFP suggest that a NTD is present and further testing is indicated. | • Ultrasound can detect a splaying of the pedicles and the classic “lemon and banana signs.” • High-resolution ultrasounds and amniocentesis • Fetal MRI |
| Spina Bifida Occulta | • Bony defect with no herniation of meninges or nervous elements • Incidental finding in 5% to 36% of adults; a small percent can develop clinical findings | • Can be associated with pigmented nevus, angioma, hairy patch, dimple, and dermoid sinus • Usually found in the lumbosacral/sacral segments • Can have associated tethered cord • May have bowel and bladder involvement |
| Spina Bifida Cystica | • Bony defect with herniation of spinal canal elements. • Meningocele | |
| Meningocele | - herniation of the meninges, but does not contain neural tissue • Usually normal neurological exam • No association with hydrocephalus or Chiari malformation • Uncommon—occurs less than 10% | |
| Spina Bifida Cystica | • Meningomyelocele | |
| Meningomyelocele | - herniation of meninges and neural elements • Most common • Associated with hydrocephalus and Chiari type 2 malformations • Abnormal motor and sensory exam • Neurogenic bowel and bladder • 75% in the lumbosacral segment | |
| RACHISCHISIS | • Occurs when the neural folds do not join at the midline and the undifferentiated neuroectoderm remains exposed. • Severe defect with exposure of the brain, spinal cord and meninges | |
| OCCULT SPINAL DYSRAPHISM | • Myelodysplasia • Implies more significant forms of closed spinal cord malformations (ex. syringomyelia, diastematomyelia, lipoma of the conus medullaris, tethered cord) | • Most cases have normal skin overlying the NTD or may have hemangioma, pit, lump, hairy patch • Symptoms maybe absent or minimal static or slowly progressive |
| Myelodysplasia | = Disorder of secondary neurulation | |
| TETHERED CORD | • Abnormal attachment of the spinal cord at its distal end. • All children born with spina bifida have a low-lying cord, and approximately one-third develop neurologic, urologic, or orthopedic complications or symptoms. | • Second most common cause of neurologic decline in a child with myelomeningocele. |
| TETHERED CORD symptoms | • spasticity in the lower extremities, decline in lower extremity strength, and worsening scoliosis. • Back pain, changes in urologic function, changes in gait, and development of lower extremity contractures. | |
| Normal spinal cord | end of spinal cord | |
| Lipomeningocele | spinal cord attached to fatty growth | |
| Attached to scar tissue | spinal cord attached to scar tissue | |
| CAUDAL REGRESSION SYNDROME | • Absence of the sacrum and portions of the lumbar spine • Associated with maternal diabetes | • Associated findings include syringomyelia, anorectal stenosis, renal abnormalities, external genital abnormalities, and cardiac problems • Motor and sensory abnormalities |
| DIASTEMATOMYELIA | • Postneurulation defect that results in a sagittal cleavage of the spinal cord, most commonly affecting the lumbar and thoracolumbar levels of the spinal cord. • It is more common in females | • May present in childhood or, less commonly, in adulthood. |
| DIASTEMATOMYELIA Orthopedic symptoms | include scoliosis, Sprengel’s deformity (especially when associated with Klippel-Feil sequence), hip subluxation, and lower extremity limb-length discrepancies. | |
| DIASTEMATOMYELIA | gait abnormalities, asymmetric motor and sensory deficits of the lower extremities, and neurogenic bladder and bowel. | |
| SYRINGOMYELIA 1 | • A tubular cavitation in the spinal cord parenchyma extending more than two spinal segments • Present in up to 40% of individuals with myelomeningocele. | • The syrinx may be located anywhere along the spinal cord, medulla, or pons, but is most common in the cervical region. • Associated with Arnold-Chiari malformation |
| SYRINGOMYELIA 2 | • If a patient develops decreasing function above the level of their lesion, syringomyelia must be considered in the differential diagnosis. • Early progression of scoliosis above the initial neurologic level may be the earliest sign of a syrinx. | • A shunt malfunction may contribute to a symptomatic syrinx, and shunt function should be evaluated. |
| CUTANEOUS LESIONS ASSOCIATED WITH OCCULT SPINAL DYSRAPHISM • Imaging Required | ▪Subcutaneous mass or lipoma ▪Hairy patch ▪Dermal sinus ▪Atypical dimples > 5 mm deep > 25 mm from the anal verge ▪Vascular lesions ( hemangioma, telangiectasia) ▪Skin appendages or polypoid lesions (e.x skin tags) ▪Scar-like lesions | |
| CUTANEOUS LESIONS ASSOCIATED WITH OCCULT SPINAL DYSRAPHISM • Imagine Not Required | Simple dimples < 5 mm or < 25 mm from the anal verge Coccygeal pits | |
| CUTANEOUS LESIONS ASSOCIATED WITH OCCULT SPINAL DYSRAPHISM • Imaging Uncertain | ▪Hyperpigmented patches ▪Deviation of gluteal fold | |
| SYRINGOMYELIA CLINICAL SIGNS 1 | • Motor and sensory deficits vary according to the level and extent of spinal cord involvement. • Spinal cord involvement may result in asymmetric motor and sensory deficits. | • Sensory deficits usually follow a dermatomal pattern and may not affect all sensory modalities equally. • Neurogenic bladder and bowel dysfunction may be present in all patients because of the distal level of innervation of the bladder and bowel. |
| SYRINGOMYELIA CLINICAL SIGNS 2 | • Musculoskeletal deformities related to muscle imbalance may present serious clinical concerns. • Latex allergy* | |
| In the care of spina bifida patients, two levels are often described: | the anatomic level of the lesion and the neurologic level of functional involvement. | |
| Trunk | T6-12 • Abdominals • Trunk flexion • Lower trunk extensors | |
| Hip | L1, L2, L3 • Iliopsoas hip flexion • Hip adductors | |
| Hip | L4, L5,S1 • Gluteus medius • Hip abduction | |
| Hip | L5, S1,S2 • Gluteus maximus • Hip extension | |
| Knee | L2, L3, L4 • Quadriceps • Knee Extension | |
| Knee | L4, L5, S1, S2 • Hamstring-hip extension • Knee flexion | |
| Ankle | L4, L5, S1 • Tibialis anterior • Dorsiflexion, inversion | |
| Ankle | L5, S1 • Peroneal Eversion | |
| Ankle | L4?, L5, S1, S2 • Triceps surae • Plantar flexion | |
| Ankle | L5, S1, S2 • Tibialis posterior • Plantar flexion, inversion | |
| Foot | L4, L5, S1 • Toe extensors | |
| Foot | L5, S1, S2 • Toe Flexors | |
| Foot | L5, S1, S2 • Foot intrinsics | |
| Perineum | S2, S3, S4 •Perineum sphincters | |
| T6-12 | • Complete leg paralysis • Kyphosis • Scoliosis • Hip, knee flexion contractures • Equinus foot • Bowl and bladder dysfuntion | |
| L1, L2, L3 | • Early hip dislocation • Hip flexion and adduction contractures • Scoliosis • Lordosis • Knee flexion contractures • Equinus foot • Bowel and bladder dysfunction | |
| L4, L5 | •Late hip dislocation • Scoliosis, lordosis • Calcaneovarus or calcaneus foot • Knee extension contractures • Bowel and bladder dysfuntion | |
| S1, S2 | • Cavus foot • Bowel and bladder dysfuntion | |
| S3, S4 | • Cavus foot • Bowel and bladder dysfuntion | |
| SPINAL CORD | Tethering Distal focal abnormalities Thick, short filum terminale Supernumerary fibrous bands Lumbosacral tumors (lipoma, fibrolipoma, fibroma dermoid, epidermoid cyst, teratoma) Bony vertebral ridge Diastematomyelia, diplomyelia, split cord | |
| BRAINSTEM | Arnold type Il malformation Kinking, inferior displacement of medulla Herniation into cervical spinal canal Abnormalities of nuclear structures Dysgenesis, hypoplasia, aplasia, defective myelination Hemorrhage, ischemic necrosis Syringobulbia | |
| CEREBELLUM | Arnold-Chiari type II malformation Elongated vermis, inferior displacement Herniation into cervical spinal canal Abnormal nuclear structures Dysplasia, heterotopia, heterotaxia | |
| VENTRICULAR SYSTEM | Hydrocephalus Aqueductal stenosis, forking, atresias | |
| FOREBRAIN | Polymicrogyria Abnormal nuclear structures Heterotopia (subependymal nodules) Heterotaxia Prominent massa intermedia Thalamic fusion Agenesis of olfactory bulbs and tracts Attenuation/dysgenesis of corpus callosum | |
| CHIARI TYPE II | • The most common hindbrain abnormality in neural tube defects • Seen in 80% to 90% of individuals with myelomeningocele • Almost always associated with hydrocephalus. • Signs of bulbar compromise arise from compression of the herniated hindbrain. | • Caudal displacement of the medulla may occur and result in traction neuropathies of the lower cranial nerves. • Only 20% will develop clinical signs of brainstem dysfunction, with most occurring in the neonatal period. |
| CHIARI TYPE II results | caudal displacement or herniation of the medulla, lower pons, elongated fourth ventricle, and cerebellar vermis into the cervical spinal cord. | |
| CHIARI TYPE II symptoms | may be evident at birth or present within the first two to three months. | |
| CHIARI TYPE II | • Most severe symptom is respiratory compromise • Dysphagia and extraocular motion abnormalities may also relate to other cranial neuropathies • If brainstem is compromise, hemiparesis or tetraparesis may be seen (more common in older children/adults) | • Control of ocular motility is related to cerebellar function (saccadic eye movements, visual fixation, and pursuit). • Despite successful initial treatment with surgical decompression, problems may recur. |
| CHIARI TYPE II Individuals may experience | stridor, laryngeal nerve palsy with vocal cord paralysis, upper airway obstruction, periodic breathing, central or obstructive sleep apnea, or aspiration. | |
| HYDROCEPHALUS prevalence in individuals with myelomeningocele | reported to be as high as 95%, with shunt rates ranging from 77% in the 1980s to 58% in more recent years. | |
| HYDROCEPHALUS symptoms | include those that are classic for increases in intracranial pressure. | |
| HYDROCEPHALUS In an infant, | signs of increased intracranial pressure include lethargy, decreased feeding, bulging fontanelle, increasing head circumference (greater than expected for age), poor developmental progress, and “sun downing.” | |
| HYDROCEPHALUS In patients with a closed fontanelle, | signs of increased intracranial pressure include headache, vomiting, drowsiness, changes in behavior, changes in personality, irritability, diplopia, and papilledema. | |
| HYDROCEPHALUS | • With the sudden onset of increased intracranial pressure, Cushing’s triad (progressively increasing systolic blood pressure, bradycardia, and irregular respirations) may be seen. | • At present, placement of a shunt is standard of care for surgical management of hydrocephalus. |
| Endoscopic management of hydrocephalus such as endoscopic third ventriculostomy (ETV) | provides direct communication between the third ventricle and the subarachnoid space by way of interpeduncular and prepontine cisterns. | |
| Polymicrogyria | increased numbers of small-sized cerebral gyri with shallow disorganized sulci, and this is seen in up to 65% of individuals. | |
| Heterotopias | are aberrant neural tissues in the form of subependymal nodules. They are present in approximately 40% of cases | |
| FOREBRAIN MALFORMATIONS | • Polymicrogyria • Heterotopias • Dysgenesis or agenesis of the corpus callosum | • Microscopic studies have demonstrated disordered cortical lamination, neuronal hypoplasias of the thalamus, and complete or partial agenesis of the olfactory bulbs and tracts. |
| Dysgenesis or agenesis of the corpus callosum | may be seen and may also be associated with a malformed cingulated gyrus and septum pellucidum. | |
| Vertebral anomalies | contribute to progressive kyphosis and scoliosis. | |
| Thoracic deformities | may result from rib deformities, including absence, bifurcation, or reduction of the ribs. | |
| Malformations of the urinary system | result in accelerated deterioration of renal function. | |
| Neural tube defects | have been associated with genetic abnormalities, including trisomy 18, trisomy 13, Turner’s syndrome, Waardenburg’s syndrome, renal aplasia and thrombocytopenia syndrome, nail–patella syndrome, deletion 13q syndrome, and others. | |
| TREATMENT | • Team: neurosurgery, orthopedic surgery, urology, rehabilitation medicine, physical and occupational therapy, social work, nutrition, and nursing | |
| REHABILITATION - Musculoskeletal • PROM exercise | is applied to all joints below the level of paralysis, with special emphasis on joints with evident muscle imbalance. | |
| REHABILITATION - Musculoskeletal • The infant | should not lie constantly in one position, but should be moved and turned frequently. • Encouraging “back to sleep”,“prone to play” | |
| REHABILITATION - Musculoskeletal • Splints | must be used with great precaution, removed frequently to check for skin irritation, and adjusted or discontinued if such problem occurs. | |
| REHABILITATION - Musculoskeletal • PROM and splints | are advisable after surgical correction of deformities to maintain joint mobility gained by the procedure. | |
| REHABILITATION - Musculoskeletal • Strengthening exercises | are sometimes beneficial for partially innervated muscles or after surgical muscle transfer for improving strength or function. They are also part of ambulation training with upper extremity assistive devices. | |
| REHABILITATION - Musculoskeletal • Consistently maintained hip flexion, | particularly when passive extension is incomplete, is a sign of hip extensor weakness. | |
| REHABILITATION - Musculoskeletal • Palpation of muscle bulk | is helpful because atrophy may be evident with severe or complete paralysis in particular muscles. | |
| REHABILITATION - Musculoskeletal • In assessing motor or sensory function, | the presence of spinal reflex withdrawal or triple flexion of hip, knee, and ankle should not be mistaken for voluntary motion and preserved sensation, particularly in high spinal lesions. | |
| REHABILITATION - Musculoskeletal • A normal asymmetric tonic neck reflex elicited in the arms without response in the legs | suggests lower extremity paralysis. | |
| REHABILITATION NEEDS BY FUNCTIONAL MOTOR LEVEL Thoracic | Expected Muscle Function: Abdominals, paraspinals, quadratus lumborum Functional Mobility: Nonfunctional ambulation/standing during therapy, school or at home, wheelchair for mobility | Equipment use: Standing frame, wheelchair, parapodium Orthotic use: Trunk-hip-knee-ankle-foot orthosis |
| REHABILITATION NEEDS BY FUNCTIONAL MOTOR LEVEL High Lumbar L1-L3 | Expected Muscle Function: Hip flexion, hip adduction Functional Mobility: Limited household ambulation, wheelchair for mobility Equipment use: Wheelchair, walker, forearm crutches Orthotic use: Reciprocating gait orthosis, hip-knee-ankle-foot orthosis | |
| REHABILITATION NEEDS BY FUNCTIONAL MOTOR LEVEL Midlumbar L3-L4 | Expected Muscle Function: Knee extension Functional Mobility: Household, limited community ambulation Equipment use: Wheelchair, walker, forearm crutches Orthotic use: Knee-ankle-foot orthosis | |
| REHABILITATION NEEDS BY FUNCTIONAL MOTOR LEVEL Low lumbar L4-L5 | Expected Muscle Function: Hip abduction, knee flexion, ankle dorsiflexion, ankle inversion, toe extension Functional Mobility: Household, community ambulation, wheelchair for long distances | Equipment use: Wheelchair, forearm crutches Orthotic use: Ankle-foot orthosis |
| REHABILITATION NEEDS BY FUNCTIONAL MOTOR LEVEL Sacral S1 S2 | Expected Muscle Function: Hip abduction, knee flexion, ankle dorsiflexion, ankle inversion, toe extension Functional Mobility: Community ambulation Equipment use: --- Orthotic use: Supramalleolar othosis, foot orthosis | |
| Mobility | can be achieved through various means, including selfpropulsion, adapted equipment, and orthotics. | |
| AMBULATION/MOTILITY | • Introduction of dynamic standers can be done early in thoracic and high lumbar levels. These include mobile prone stander, Parapodium, and swivel walkers. • Casting | • Wheelchair mobility should be introduced to all children who will potentially use this as a primary or secondary option. |
| ORTHOPEDIC COMPLICATIONS | • Spinal deformities • Hip subluxation and dislocation • Lower extremity contractures, foot deformities • Fractures • Osteoporosis | |
| MEDICAL COMPLICATIONS | • Hypertension, overweight, obesity, and metabolic syndrome • Sleep-related breathing disorders • Short stature • Precocious puberty • Neurogenic bladder and bowel | |
| SELF CARE • Children with spina bifida | should be encouraged to acquire independence in age-appropriate activities of daily living (ADLs) at an early age. | |
| SELF CARE • Family members | should be instructed to proceed with age-appropriate expectations. | |
| SELF CARE • If there are continuing problems and extensive lower extremity paralysis, | an occupational therapy consultation is necessary; this should include education of the child and the parents. | |
| TREATMENT • Toddlers (age 1–3 years) | require about 500 mg of calcium each day. | |
| TREATMENT • Preschool and younger school-age children (age 4–8 years) | require about 800 mg of calcium each day. | |
| TREATMENT • Older school-age children and teens (age 9–18 years) | require about 1300 mg of calcium each day. | |
| TREATMENT • It is now recommended that all infants and children, including adolescents, | have a minimum daily intake of 400 IU of vitamin D beginning soon after birth. | |
| TREATMENT • Weight- bearing activities | should be encouraged. | |
| TREATMENT • Treatment for pathologic fractures | supports the use of medication such as bisphosphonates. | |
| COGNITIVE FUNCTION • Spina bifida | has long been associated with specific neuropsychological characteristics marked by deficits in nonverbal learning abilities, including math concepts, visual–spatial perception, spatial reasoning, and time concepts; | processing speed, organization, and personality traits and; verbal skills. |
| COGNITIVE FUNCTION • Those who have hydrocephalus and multiple shunt revisions | may have more impairments than those who do not. | |
| COGNITIVE FUNCTION • Deficits | can be in multiple domains and include visual-spatial, perceptual motor, organization, executive function, sequencing, memory, attention, or just about any other type of learning problem | |
| TREATMENT OF NONVERBAL LEARNING DISORDER | • Identification of the learning disorder is critical. Testing should be done prior to entrance into school. • Modified program to address these specific needs. • Providing structure and direction for education. Be specific and repetitive. | • Teach step-wise and sequentially (baby steps). • Make sure to teach social education, as these children may not pick up social cues. • Use multiple sources available on NVLD for guide in education, selfskills training, and social integration. |
| AGING WITH A NEURAL TUBE DEFECT • Spina bifida | is associated with abnormalities in the brain and spinal cord. | |
| AGING WITH A NEURAL TUBE DEFECT • ventricular–peritoneal shunts. | Approximately 90% of adults will have this | |
| AGING WITH A NEURAL TUBE DEFECT • Shunt malfunctions | can occur at any age and can lead to significant morbidity, mortality, and sudden death. | |
| AGING WITH A NEURAL TUBE DEFECT • Adult-onset tethered cord | should be considered in a deterioration of neurologic status, bowel or bladder changes, increasing orthopedic deformities, and gait deviations | |
| AGING WITH A NEURAL TUBE DEFECT • Spinal deformities, including scoliosis, kyphosis, and lordosis, | can increase over time and cause back pain. | |
| AGING WITH A NEURAL TUBE DEFECT • Chronic lack of sensation and muscle imbalances | can lead to Charcot joints. | |
| AGING WITH A NEURAL TUBE DEFECT • Overuse syndromes | are common in wheelchair and crutch users. | |
| AGING WITH A NEURAL TUBE DEFECT • Gait abnormalities from underlying muscle weakness | can cause undue stress on joints in the lower extremities. | |
| AGING WITH A NEURAL TUBE DEFECT • Neurogenic bowel and bladder function | is an important component of adult medical care. | |
| AGING WITH A NEURAL TUBE DEFECT • Aging | causes changes in fat and muscle distribution, which can affect pressure ulcer formation. | |
| AGING WITH A NEURAL TUBE DEFECT • bracing | • In the lower extremities can cause pressure and shear over bony prominences. | |
| AGING WITH A NEURAL TUBE DEFECT • The wheelchair seated position | results in pressure in the ischial and sacral areas. | |
| AGING WITH A NEURAL TUBE DEFECT • Obesity | is a health-related problem for both able- bodied and disabled adults. | |
| AGING WITH A NEURAL TUBE DEFECT • Sexuality and sexual function | is often overlooked in the disabled population. | |
| VOCATIONAL COUNSELING • Functional vocational planning | should be started early in secondary school, assessing career interests, skills, and aptitude. | |
| VOCATIONAL COUNSELING • The potential for success in a postsecondary school program | should be explored along with vocational job training. | |
| VOCATIONAL COUNSELING • A positive realistic approach | may provide the best solution in planning for adult employment options. |
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